The adult lung continually synthesizes collagen but the total amount of collagen present remains constant. Thus, mechanisms must be present for the continued breakdown of collagen to match this rate of synthesis. Two mechanisms of lung collagen degradation are being evaluated: (1) extracellular degradation via collagenase secreted by alveolar macrophages, monocytes, polymorphonuclear leukocytes and fibroblasts; and (2) intracellular degradation by lung explants and fibroblasts. Both mechanisms appear opperant in lung and they may be critical control points in modulating the presence of lung collagen in normals, pulmonary fibrosis and emphysema.